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P2–207: CSF beta‐amyloid 1–42, but not CSF tau, phosphorylated tau or hippocampal atrophy on MRI relate to Alzheimer's disease pathology load in the brain
Author(s) -
Bouwman Femke,
Schoonenboom Niki,
Vrugte Sabine,
Bechten Arianne,
Barkhof Frederik,
Rozemuller Annemieke,
Visser Pieter Jelle,
Teunissen Charlotte,
Scheltens Philip,
Van der Flier Wiesje
Publication year - 2013
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2013.05.853
Subject(s) - atrophy , pathology , autopsy , medicine , biomarker , hippocampal formation , alzheimer's disease , amyloid beta , hippocampus , cerebrospinal fluid , temporal lobe , neuroscience , psychology , disease , chemistry , biochemistry , epilepsy
Plaque density was most notable with Ab staining, followed by subsequent decreases of BuChE and thioflavin-S plaque staining. Conclusions: The Leu235Pro substitution of the PSEN1 gene produces significant behavioral and pathological impairment, with onset typically before 40 years of age. As reported in cases of sporadic AD, these findings confirm that BuChE is highly associated with AD pathology in this mutation and may be involved in the maturation of toxic Ab protofibrils. This enzymemay hold promise as a therapeutic and neuroimaging target in AD, particularly in cases of aggressive FAD forms.